Professional Documents
Culture Documents
Electrolytes
Electrolytes
⬇️
intake: ● Relaxes muscles in skeletal and cardiac ➢ Water is being pulled out of cell causing it to shrink
2.5g/day during na-k pump ● Consumption ➢ Dehydrated!
● Does not cross the wall ● Diuretics “thiazides” ➢ Develops from an excess water loss, frequently
● Regulated by ADH, thirst, and RAAS ● Vomiting, GI suction accompanied by impaired thirst mechanisms
● Diarrhea, sweating ➢ High aldosterone level
● Addison’s Disease
○ Low aldosterone Causes:
●
○ Needed in maintaining blood pressure
Damage to adrenal glands
●
○ ⬆️
Cushing Syndrome
cortisol - ⬆️ ⬇️
Na; K
●
○ ⬆️
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Secretion of ADH
●
○
○
⬆️
Conn’s Syndrome
Aldosterone
independent and excessive aldosterone
○ Water is being kept
■ This dilutes the sodium production in the adrenal cortex
■ Common in px with heart failure ○ Potential for hypokalemia
○
■ Risk for hypovolemia
Oversecretion of vasopressin
●
●
○ ⬇️
Corticosteroids
Intake of water
Diabetes Insipidus
● Fluid overload
● Cardiac/Congestive HF ●
⬆️
Burns
⬆️
⬆️
● Renal failure ● Intake of Na
● Hypotonic solutions ● Hypertonic solutions
● Hyperactive bowel sounds ● Encephalopathy of any cause or cerebrovascular dx
○ Fluid moves from a lower concentration to a higher ● Hyperthermia, delirium, and coma
concentration. Since there is hyponatremia
○ Inc peristalsis
Chloride (Cl) ●
●
Associated with Na
Acid-base balance (bicarb)
HYPOCHLOREMIA
● GI related: vomiting, gastric juice, ileostomy ● ⬆️
HYPERCHLOREMIA
Na intake (hypertonic fluids)
98-106 mEq/L ●
●
●
Digestion (Hcl)
Balances fluid with Na
Major ECF anion
●
●
●
Diuretics “thiazides”
Burns
Cystic fibrosis!!!
●
●
●
⬇️
Water draining / losing too much water
Bicarb (loss during diarrhea)
Conn’s syndrome
●
● Bicarb,
○
⬇️
Metabolic alkalosis
chloride
They have an opposite relationship
●
●
Corticosteroids
Metabolic acidosis
○ Similar with hyponatremia and acidosis
● Fluid overload
● Heart failure or SIADH
Potassium (K)
3.5-5.0 mEq/L
●
●
●
⬆️ ⬇️ ⬆️ ⬇️
Has opposite relationship with sodium
Na = K; K= Na
Found mainly inside the cell
HYPOKALEMIA
● Loop diuretics, corticosteroids, too much insulin
○ Too much insulin moves k into cell
HYPERKALEMIA
● Movement in and out of the cell
○ Due to burns and tissue damage
● Sodium is located outside (mainly) ● Cushing’s syndrome ○ Massive cell destruction!!!!
● Muscle contraction ● Starvation, losing too much K (vomiting/GI disturbances) ● Rhabdomyolysis (breakdown of muscles)
● Nerve impulse ● ST depression, inverted T wave, and prominent U wave ●
⬇️
Addison’s disease
○ aldosterone
■ Excreted Na but keeps K
● Renal failure
● K-sparring, ace inhibitors, nsaids
“Seven Ls ” “MURDER”
L Lethargic
L Low, shallow respirations M Muscle weakness
L Lethal cardiac dysrhythmias U Urinary output (little to none)
L Lots of urine R Respiratory failure
L Leg cramps D Decreased cardiac contractility
L Limp muscles E Early muscle twitches/cramps
L Low BP and heart R Rhythm changes
→ tall, peaked T waves
→ prolonged PR interval
Calcium (Ca)
9-10.5 mg/dL
●
●
●
Bones / teeth
Muscles, nerves, clotting
Absorbed in GUT
●
●
⬇️
HYPOCALCEMIA
⬇️
PTH due to surgery
Intake (lactose intolerant peeps)
HYPERCALCEMIA
●
● ⬆️
Hyperactive PTH → releases too much CA
Vit D supplements intake
2.25-2.75 mmol/L Bones release Ca+ in the blood if there;s ● Low vitamin d ● Cancer spreads in bones which make it weaker
hypocalcemia and it weakens overtime ● Chronic kidney disease ● Thiazides, lithium = PTH are affected
Bound ● Bisphosphonates ● Tetany
● attracted to Factors in absorption: ○ Slows down the ability of the bones to release Ca ● Hypoactive bowel sounds
CHON ➢ Vitamin D into the blood ● Hypoactive deep tendon reflex
(albumin) ➢ PTH (Parathyroid) ○ It makes the bones stronger and avoids
➢ Calcitonin (Thyroid) osteoporosis
Ionized: ● Aminoglycosides “mycin”
● “Free” Ca ○ It wastes Ca via kidneys
● Active form ● Anticonvulsants
● Ecf ○ Affects vitamin D in the body
Trousseau’s sign Chovostek’s sign
“CRAMPS” “WEAK”
C Convulsions
R Reflexes are hyperactive W Weakness of muscles
E EKG changes
A Arrhythmias A Absent reflexes
→ prolonged QR interval Affected mental state
M Muscle spasms Abdominal distention
→ in calves and feet (tetany) K Kidney stone formation
P Positive signs
⇒ Trousseau’s sign
⇒ Chovostek’s sign
Paresthesia
S Sensation of tingling/numbness
(paresthesia)
→ Excitement → Weakened
Magnesium (Mg)
1.3-2.1 mg/dl
●
●
●
Mainly located in ICF
Nerve, muscles, vessels
It makes the muscles relaxed and acts on ●
⬇️
HYPOMAGNESEMIA
● mg intake
Other electrolyte imbalance (K/Ca)
HYPERMAGNESEMIA
● Rare; this is due to trying to correct hypomagnesemia or
during labor and delivery
0.65-1.05 mmol/L blood vessels to maintain blood pressure ● Small intestine malabsorption ● Mothers are given magnesium sulfate during L & D
● Has a role in sodium-potassium pump ○ Could be caused by PPI ○ Nursing mx: monitor levels
Major anion in ECF ● Magnesium is binds with ATP ● Alcoholism ● Renal failure
○ It moves 3 Na+ out of the cell ● Malabsorption ● Receiving IV magnesium sulfate
and; ● Diabetic ketoacidosis ●
○ 2 K+ enters the cell
● Absorbed in small intestine “TWITCH” “LETHARGIC”
● Magnesium competes with calcium for the
binding spot
● No magnesium ⇒ continuous T Trousseau and Chvostek sx L Lethargic (prominent)
●
●
⬇️ Ca levels =⬇️
spasms/cramps/ contractions
Magnesium
Regulated by kidney and GIT
W Weakness
E EKG changes
→ prolonged PR/QT interval
I Inc deep tendon reflexes → widened QRS complex
T Torsades de pointes / tetany T Tendon reflexes are diminished
C Ca and K levels are low H Hypotension
ICF: A Arrhythmias
H Hypertension
● Skeletal muscle contractions, CHON
R Red/hot face
metabolism, ATP formation, Vit-B Complex
activation, DNA synthesis , CHON G GI issues
synthesis I Impaired breathing
C Confusion
ECF:
● Regulates blood coagulation & skeletal
contractility
Phosphate and
○ Parathyroid gives signals to
kidney to inhibit absorption of
phosphate ●
○ ⬆️
amount of food causing increased insulin
BS → phosphate is then needed
Overactive parathyroid
●
●
●
Rhabdomyolysis : renal damage
Hyperparathyroidism
Chemotherapy
Calcium works in ● Vitamin D influence phosphate absorption ○ Inhibits kidney absorption of phosphate
opposite way ○ Low vitamin d levels S/sx
➢ Same with hypocalcemia
“BONE” ➢ Convulsions
➢ Reflexes are hyperactive
➢ Arrhythmias
B Bone pain / fracture ➢ Muscle spasms
O Osteomalacia ○ Calves / feet, tetany, seizures
→ bone softening/ leg bowing ➢ Trousseau and Chovestek’s sx
→ Rickets = short people
N Neuro status changes
→ irritable, confused, seizures
E Erythrocyte destruction
HYPOVOLEMIA HYPERVOLEMIA
● Loss of ECF volume exceeded the intake of fluid ● High volume of water in the IV compartment
● ECF loss > fluid intake ○ Too fast IV infusion: pulmonary congestion/ pulmonary edema
○ Inadequate fluid intake ● Excessive oral intake, rapid IV infusion
○ Hemorrhage ● Heart failure. Kidney disease
○ Prolonged vomiting and diarrhea ● Excessive salt intake
○ Wound loss (burn injury) ● Administration of corticosteroids
○ Profuse urination or perspiration ● CVP: >10cm H2O
○ Translocation of fluids in abdominal cavity
● Hemoconcentration
○ Increased potential for blood clots, urinary stones
● Depletes ICF which can affect cellular functions = change in mental state
● Third-space fluid shifts , diabetes insipidus, adrenal insufficiency
● Osmotic diuresis, coma, diuresis, urination
● Hemorrhage
● Reabsorption
● ECF loss
Assessment Assessment:
➢ Thirst (earliest sx) ● Weight gain, elevated BP, increased breathing effort
➢ ⬇️ ⬆️
➢ Weight loss of >2lb/24hr
BP, T
➢ Rapid, weak, and thready pulse
●
●
●
Dependent edema
Prominent jugular vein when sitting
Moist breath sounds (pulmonary congestion)
➢ Rapid and shallow respiration
➢ Scant and dark yellow urine Dx:
➢ Dry and small volume stool ● Hemodilution
➢ Warm and flushed skin , tented skin turgor, sunken eyes, clear lungs ○ Low blood cell count, low hematocrit
➢ Effortless breathing, weakness, flat jugular veins, reduced cognition, sleepy ● Low urine SG
➢ Dry mouth ● CVP greater than 10cm
Function of bicarbonate:
● Maintains acid-base balance by functioning as primary buffer